Medication Overuse Headache: Diagnosis & Treatment

Risk Factors

There appear to be both environmental and genetic risk factors for the development of MOH. Smoking and sedentary lifestyle are associated with a more than double risk of MOH.4 There is a clear association between psychiatric comorbidities such as anxiety and depression, but whether these are a cause or effect of MOH is not clear.5 Certain habits and underlying personality traits may also be risk factors. Specifically, cephalalgiaphobia, or the fear of headache may result in increased use of abortive medications leading to MOH.4 The use of caffeine, including the use of analgesics that contain caffeine, is also linked to the chronification of headache.6

Additionally, men and women may have different sensitivities to specific agents. Opiates appear to have a stronger relationship with MOH in men and barbiturates in women.5 Polymorphisms in the MTHFR,7 Dopamine Receptor D2 (DRD2),7 COMT,8 SLC6A4,8 and RAMP18 genes have all been linked with a higher likelihood of chronification of headache.


The treatment of medication overuse headache is often multi-faceted and patient dependent. The most important step is cessation of the offending agent or agents. Strategies for cessation of the medication at fault can differ depending on the medication class, duration, and dose being used by the patient. Simple analgesics such as ASA, acetaminophen, and NSAIDs can typically be discontinued immediately. Likewise, triptans and ergotamines can be stopped immediately, and these patients may actually recover more quickly than other types of MOH. When opiate medications or barbiturates are implicated in MOH, cessation may require a prolonged taper and rarely inpatient detoxification. For more refractory cases, pain rehabilitation programs can also be beneficial.9

Upon cessation of the offending agent, additional treatment is usually required to bolster the effect, mitigate withdrawal symptoms, and increase compliance. In general, there are 2 strategies which are often used concurrently. Some patients will require bridging therapy of a long acting NSAID or short taper of an oral steroid which is started simultaneously with a longer term prophylactic agent .10 The most studied prophylactic agents in MOH are topiramate11 and onabotulinum toxin A,12 however other migraine prophylactic agents may be entirely appropriate depending on the patient. Non-medication approaches such as biofeedback13 and cognitive behavioral therapy may be helpful adjunct therapies and may help with more long term coping strategies.

The ultimate goal of treatment in MOH is to revert to a pattern of episodic headache more in keeping with the patient’s primary headache disorder. When an episodic pattern is achieved, it is paramount for the patient to have instruction in proper use of abortive medications to avoid recurrence.

Will Kingston, MD, completed his undergraduate degree in Biology at Queen’s University in Kingston, Ontario and attended medical school at Saba University School of Medicine in Saba, Netherlands Antilles. He completed his residency in neurology at the University of Toronto, where he served as chief resident. Dr Kingston is currently enrolled in a headache medicine fellowship at Mayo Clinic Arizona.

Rashmi Halker, MD, FAHS, is an Assistant Professor of Neurology at Mayo Clinic and a Fellow of the American Headache Society. She attended medical school at Wayne State University in Detroit before completing a residency in neurology and fellowship in headache medicine at Mayo Clinic in Phoenix, Arizona.  Dr Halker is a headache medicine subspecialist at Mayo Clinic, and is also the chair of the Women’s Issues SIG for the American Headache Society.


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This article originally appeared on Neurology Advisor